| Literature DB >> 30122514 |
Sophelia Hoi Shan Chan1, Nens van Alfen2, Inger Johanne Thuestad3, Janice Ip4, Angel On-Kei Chan5, Christopher Mak6, Brian Hon-Yin Chung6, Aad Verrips7, Erik-Jan Kamsteeg8.
Abstract
We describe four unrelated patients with the same de novo heterozygous missense mutation c.751C>T in the DYNC1H1 gene. We found a high phenotype-genotype correlation with all four patients having early childhood-onset predominant lower limb muscle weakness and wasting which was slowly progressing and later-onset mild upper extremities proximal weakness. All four patients presented minor cognitive dysfunction with learning difficulty and developmental behavioural comorbidities with mild abnormalities in the brain MRI. The leg muscle MRI findings are highly consistent in DYN1CH1-related spinal muscular atrophy with lower limb predominance (SMALED) with relative sparing of biceps femoris and semitendinosus, and hypertrophy of adductor longus in the thighs; and sparing the anterior and medial muscles in the calves. This report provides important clinical evidence indicating the de novo heterozygous missense mutation c.751C>T in the DYNC1H1 gene is pathogenic causing SMALED. Muscle MRI is more specific than muscle biopsy in the diagnosis of SMALED.Entities:
Keywords: Brain MRI; Dynein cytoplasmic 1 heavy chain 1 (DYNC1H1) gene; Muscle MRI; Spinal muscular atrophy with lower extremity predominance (SMALED)
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Year: 2018 PMID: 30122514 DOI: 10.1016/j.nmd.2018.07.002
Source DB: PubMed Journal: Neuromuscul Disord ISSN: 0960-8966 Impact factor: 4.296